The respiratory system is the organ system responsible for gas exchange, conducting air through the airways to the alveoli where oxygen is absorbed into the blood and carbon dioxide is expelled from the body.

Respiratory System: Introduction — CFB (MED03) Comprehensive Exam-Ready Notes

"Patient comes to see you with a complaint of discomfort, i.e. with a symptom. You will take steps: to make the diagnosis (3 steps) → to manage." ^[1]

Step	What You Do	What You Get
1. History	Ask structured questions	Symptoms
2. Physical Examination	Look, feel, listen on the patient	Signs
3. Investigations	Order targeted tests	Objective data

Why this matters: These three steps are sequential and complementary. History narrows the differential to 2–3 likely diagnoses. Examination refines it further. Investigations confirm and quantify. Examiners test whether you can do all three systematically — skipping straight to investigations is a classic mistake that loses marks.

2. History Taking — Detailed Breakdown

The structure is: Chief Complaint (+ duration) → HPI → Past Health → Personal/Social History (TOCC, smoking, alcohol) → Family History → Drug History ^[1]

Component	Content	Why It Matters
Chief Complaint (CC)	One-liner + duration	Frames entire workup
HPI	About CC (character, severity, timing, aggravating/relieving), systemic enquiry, associations, progress, complications	Narrows the DDx
Past Health	Previous lung disease (TB, asthma), surgery, co-morbidities	Old TB → bronchiectasis, destroyed lung; DM → ↑infection risk
Personal/Social Hx	TOCC, smoking (pack-years), alcohol, occupation	Occupation links to silicosis, asbestosis; smoking to COPD/cancer
Family Hx	Asthma, atopy, lung cancer, alpha-1-antitrypsin deficiency	Genetic predisposition
Drug Hx	Medications causing respiratory effects	See drug table below

HPI Example (from lecture) [1]

Mr ABC, M/70. CC: Haemoptysis for two days. HPI: 2 months — increased cough with scanty sputum; 2 weeks — increased shortness of breath; 2 days — blood in sputum.

This illustrative case teaches you to present the chronological evolution of symptoms — the earliest symptom first, then the progressive worsening, and finally the presenting complaint. In exams, marks are often given for showing the tempo of the disease.

Cough & Sputum:

Acute (days): Acute viral/bacterial URTI, Acute pneumonia, Asthma

Subacute (weeks): TB, Lung cancer, Asthma

Chronic (years): COPD, Bronchiectasis, Asthma ^[1]

Time Course	Differential Diagnoses	Key Discriminators
Acute (days)	URTI, pneumonia, asthma exacerbation	Fever → infective; wheeze → asthma
Subacute (weeks)	TB, lung cancer, asthma	Night sweats/weight loss → TB; haemoptysis + smoker → cancer
Chronic (years)	COPD, bronchiectasis, asthma	Smoking → COPD; copious purulent sputum → bronchiectasis; episodic/reversible → asthma

Notice that asthma appears in all three categories — this is deliberate. Asthma can present acutely (exacerbation), subacutely (undiagnosed), or chronically (poorly controlled). This is an exam trap: don't pigeonhole asthma as only acute.

Drugs may cause:

Worsening of asthma/COPD: Aspirin, Beta-blockers

Increased infections (e.g. ↑ TB): Corticosteroids

Diffuse lung shadows/fibrosis: Amiodarone ^[1]

Drug	Respiratory Effect	Mechanism
Aspirin	Worsening asthma	Inhibits COX → shunts arachidonic acid to leukotriene pathway → bronchoconstriction (aspirin-exacerbated respiratory disease)
Beta-blockers	Worsening asthma/COPD	Block β2-receptors in bronchial smooth muscle → bronchoconstriction
Corticosteroids	↑ TB, ↑ infections	Immunosuppression → reactivation of latent TB; impaired neutrophil/macrophage function
Amiodarone	Pulmonary fibrosis	Direct cytotoxic damage to pneumocytes; phospholipid accumulation → inflammation → fibrosis

High Yield: Drug-Induced Respiratory Disease

These four drug-respiratory effect pairs are directly from the lecture slides and are commonly tested. If asked "name drugs that worsen asthma," answer aspirin and beta-blockers. If asked "name a drug causing pulmonary fibrosis," answer amiodarone. ^[1]

Other drugs that cause pulmonary fibrosis (from supporting material): methotrexate, bleomycin, nitrofurantoin [2, 5].

3. Physical Examination of the Respiratory System

GENERAL examination:

Respiratory distress or not

Fever

Cyanosis

Clubbing / tobacco staining

(JVP)

Oedema of legs: bilateral (cor pulmonale — RHF due to lung/pulmonary vascular disease), unilateral (DVT)

Cervical / supraclavicular lymph nodes ^[1]

Breaking this down:

Finding	What It Suggests	Clinical Reasoning
Respiratory distress	Severe/acute pathology	Use of accessory muscles, tachypnoea, inability to complete sentences
Fever	Infection (pneumonia, TB, abscess)	Must prompt TOCC
Cyanosis	Hypoxaemia (SaO2 < ~85%)	Central (tongue/lips) = low PaO2; peripheral = poor perfusion
Clubbing	See table below	Loss of Lovibond's angle → nail-bed fluctuation
Tobacco staining	Smoking history	Confirms exposure; correlates with COPD/cancer risk
JVP	Cor pulmonale, fluid overload, SVC obstruction	Raised + pulsatile = cor pulmonale; fixed/non-pulsatile = SVCO
Bilateral leg oedema	Cor pulmonale (RHF from lung disease)	Right heart fails because pulmonary hypertension ↑ afterload
Unilateral leg oedema	DVT → risk of PE	Asymmetric swelling is DVT until proven otherwise
Cervical/supraclavicular LNs	Metastatic lung cancer, lymphoma, TB	Supraclavicular = Virchow's node (left) — classic for thoracic/abdominal malignancy

Chest examination: Inspection → Palpation → Percussion → Auscultation ^[1]

Inspection:

Shape: barrel chest (hyperinflation in COPD/emphysema), kyphoscoliosis (restrictive defect) ^[1]
Scars: VATS scars (small, 1–2 cm; minimally invasive thoracic surgery), standard thoracotomy scar (posterolateral, large) ^[1]
Chest wall movement: symmetry, respiratory rate, pattern
Scoliosis — specifically shown in lecture slides as a cause of restrictive lung disease ^[1]

Palpation:

Tracheal position (midline vs deviated)
Chest expansion (reduced on affected side)
Tactile vocal fremitus

Percussion:

Percussion findings:

Resonant → normal

Dull → collapse, consolidation

Stony dull → effusion

Hyper-resonant → air (pneumothorax, emphysema) ^[1]

Percussion Note	Pathology	Why
Resonant	Normal lung	Air-filled alveoli vibrate freely
Dull	Consolidation, collapse	Solid/airless lung tissue transmits sound poorly
Stony dull	Pleural effusion	Fluid completely dampens percussion vibrations — more dull than consolidation
Hyper-resonant	Pneumothorax, emphysema	Excessive air (trapped or free) amplifies vibration

Auscultation:

Auscultation findings:

Crackles: Coarse (bronchiectasis), Fine (fibrosis) ^[1]

Sound	Character	Pathology	Mechanism
Coarse crackles	Low-pitched, early inspiratory, may clear with cough	Bronchiectasis, pneumonia	Air bubbling through secretions in dilated airways
Fine crackles	High-pitched, late inspiratory, "velcro"	Pulmonary fibrosis, early pulmonary oedema	Sudden opening of collapsed small airways/alveoli
Wheeze	Expiratory, polyphonic	Asthma, COPD	Narrowed airways vibrate during expiration
Bronchial breathing	Loud, high-pitched, equal inspiration/expiration	Consolidation	Sound transmitted efficiently through solid lung
Reduced/absent breath sounds	Quiet or silent	Effusion, pneumothorax, collapse	Sound blocked by fluid/air or no ventilation

From 2024 MCQ ^[9]:

Physical Sign	Most Likely Diagnosis
Wheezing during inspiration	Retrosternal goitre (extrathoracic upper airway obstruction)
Stony dull percussion note	Malignant pleural effusion
Bilateral fine basal crackles, JVP not raised	Idiopathic pulmonary fibrosis
Bronchial breath sound + increased vocal resonance	Pneumococcal pneumonia

Exam Intelligence: Percussion Note Discriminator

"Stony dull" = effusion. "Dull" = consolidation or collapse. Examiners specifically test whether you can distinguish these. Consolidation has dullness PLUS bronchial breathing and increased vocal resonance (because solid lung transmits sound). Effusion has stony dullness PLUS reduced/absent breath sounds and reduced vocal resonance (because fluid blocks sound). [1, 9]

4. Investigations in Respiratory Disease

Common Respiratory Investigations: Blood, Sputum, NPA, Pleural fluid, Imaging, Lung function tests, ABG/Oximetry, Bronchoscopy, Lung FNA/biopsies, Polysomnography ^[1]

Blood tests:

CBP — WBC: neutrophilia, eosinophilia

Serology — infections (e.g. viral): paired samples for antibodies in 14 days; autoimmune vasculitic disease with pulmonary presentations (e.g. SLE, RA): ANF, ds-DNA, RF etc. ^[1]

Test	What It Shows	Clinical Application
Neutrophilia	Bacterial infection	Pneumonia, lung abscess
Eosinophilia	Allergic/parasitic	Asthma, allergic bronchopulmonary aspergillosis (ABPA), eosinophilic pneumonia
Paired serology	Rising antibody titre confirms infection	Take acute + convalescent samples 14 days apart; 4-fold rise is diagnostic
Autoimmune markers	Connective tissue diseases affecting lungs	SLE (ANF, dsDNA) → pleural effusion, lupus pneumonitis; RA (RF) → ILD, pleural effusion

Sputum examination:

Gross appearance

Amount

Microscopy: Wright's stain (WBC), Gram's stain (bacteria), Ziehl-Neelsen stain (AFB/TB), Cytology (malignant cells)

Culture: Aerobic, Anaerobic bacteria; Mycobacteria; Fungi

Molecular testing ("quick" test): TB, viruses & others ^[1]

Stain	Target	Diagnoses
Wright's stain	WBC types	Neutrophils = bacterial; eosinophils = asthma/allergy
Gram's stain	Bacteria morphology	Gram +ve diplococci = S. pneumoniae; Gram -ve rods = H. influenzae
Ziehl-Neelsen	Acid-fast bacilli	TB; requires 3 consecutive early morning sputum samples
Cytology	Malignant cells	Lung cancer — especially squamous cell (central)
Culture	Organism identification + sensitivities	Guides antibiotic therapy; mycobacterial culture takes 4–6 weeks
Molecular (PCR)	Rapid detection of DNA/RNA	TB GeneXpert (result in hours vs weeks); also for viruses

Sputum characteristics as diagnostic clues (from supporting material ^[6]):

Blood-streaked → TB, lung cancer
Bloody mucopurulent → bronchiectasis, lung abscess
Pink frothy → pulmonary oedema
Rusty → pneumococcal pneumonia
Copious purulent → bronchiectasis

Pleural fluid examination:

Appearance: clear/bloody/purulent/milky

Chemistry: pH, protein, LDH

Cell counts & differential

Cytology

Microbiology

Others: e.g. adenosine deaminase (ADA) ^[1]

Light's Criteria (from supporting material — essential for exams [5, 6]):

An effusion is exudative if ANY ONE of these criteria is met:

Pleural protein / serum protein > 0.5
Pleural LDH / serum LDH > 0.6
Pleural LDH > 2/3 upper limit of normal serum LDH

Transudative	Exudative
Heart failure	Pneumonia (parapneumonic)
Cirrhosis	TB (high ADA > 40 U/L)
Nephrotic syndrome	Malignancy (positive cytology)
Hypoalbuminaemia	Empyema (purulent, pH < 7.2)

High Yield: ADA in Pleural Fluid

The lecture specifically mentions ADA (adenosine deaminase). ADA > 40 U/L in lymphocytic exudative effusion is highly suggestive of TB pleuritis in endemic areas like Hong Kong. This is a favourite exam point. [1, 5]

Thoracentesis (Chest Tapping):

Chest tapping (thoracentesis) +/- Pleural biopsy (Abram's needle). Ultrasound guidance minimises bleeding and pneumothorax. ^[1]

Plain CXR: Note that masses in the mediastinum or behind the heart may be missed. ^[1]

CT (axial cuts): picking up small nodules not detected by plain CXR; picking up mediastinal lymph nodes and masses. ^[1]

Modality	Strengths	Limitations
Plain CXR	Fast, cheap, widely available; shows consolidation, effusion, pneumothorax, masses	Misses small nodules, retrocardiac masses, mediastinal pathology
CT thorax	High sensitivity for nodules, masses, LNs, PE (with contrast)	Radiation, cost, contrast risk
CT pulmonary angiography	Gold standard for PE	Contrast allergy/renal impairment
PET-CT	Staging lung cancer (metabolically active tissue lights up)	Expensive, false +ve with inflammation

4.6 Lung Function Tests

Lung Function Tests: PFR, Spirometry (FEV1/FVC), Lung Volumes (TLC, RV), Diffusing Capacity (DLCO), ABG (pH, PaO2, PaCO2), Oximetry (SaO2) ^[1]

The lecture beautifully organises these tests by what they measure:

PFR and Spirometry → AIRWAY function
DLCO → ALVEOLAR function
ABG and Oximetry → DEFINING RESPIRATORY FAILURE ^[1]

FEV1 = Forced Expiratory Volume in 1 second; FVC = Forced Vital Capacity

FEV1/FVC ratio:

Normal: > 70%, and both FEV1 & FVC normal

Restrictive: ratio > 70%, but both FEV1 and FVC are low (e.g. fibrosis, kyphosis/scoliosis, pleural effusion)

Obstructive: ratio < 70% ^[1]

Pattern	FEV1/FVC	FEV1	FVC	Examples
Normal	> 70%	Normal	Normal	Healthy
Obstructive	< 70%	↓↓	↓ or normal	COPD, asthma
Restrictive	> 70% (or normal)	↓	↓	Pulmonary fibrosis, kyphoscoliosis, effusion

Why FEV1/FVC < 70% = obstructive: In obstructive disease (asthma, COPD), the airways are narrowed or collapse during expiration. The patient can't blow air out quickly → FEV1 drops disproportionately more than FVC → ratio falls below 70%.

Why FEV1/FVC preserved in restrictive disease: In restrictive disease, the lungs are stiff or the chest wall can't expand. Both FEV1 and FVC are reduced proportionally because the total volume of air is reduced, but the airways themselves are not narrowed → ratio stays normal or even increases.

Exam Trap: Asthma vs COPD Spirometry

Both asthma and COPD show obstructive pattern (FEV1/FVC < 70%). The discriminator is reversibility: in asthma, FEV1 improves ≥ 12% AND ≥ 200 mL after bronchodilator. In COPD, there is minimal reversibility. The 2023 minicase tested this directly with pre- and post-bronchodilator spirometry values. [1, 8]

From the 2023 minicase (Mr Chan, construction worker, smoker, old TB) ^[8]:

Pre-BD FEV1 = 1.20 L (60% predicted), FVC = 2.00 L (70%), FEV1/FVC = 60%
Post-BD FEV1 = 1.25 L (62%), FVC = 2.10 L (71%)
Interpretation: Obstructive pattern with NO significant reversibility → COPD (not asthma)
This patient also had two respiratory diagnoses: COPD + bronchiectasis (or silicosis, given construction worker history)

DLCO measures the function of alveoli. Function of respiration is gaseous exchange (O2 and CO2). ^[1]

DLCO tests the efficiency of gas transfer across the alveolar-capillary membrane. The patient breathes a small amount of carbon monoxide (CO), which has very high haemoglobin affinity, so uptake is limited only by the membrane and capillary blood volume, not perfusion.

DLCO	Condition	Why
↓↓	Pulmonary fibrosis	Thickened alveolar membrane impairs diffusion
↓↓	Emphysema	Destroyed alveolar surface area
↓	Anaemia	Less Hb to bind CO
↑	Pulmonary haemorrhage	Hb in alveoli binds CO → falsely high
↑	Polycythaemia	More Hb available

Respiratory failure is logically defined by abnormal body O2/CO2:

Low SaO2 / PaO2 = oxygenation failure (Type I)

Low PaO2 + high PaCO2 = ventilatory failure (Type II) ^[1]

Type	PaO2	PaCO2	Mechanism	Examples
Type I	Low (< 8 kPa)	Normal or low	V/Q mismatch, diffusion impairment, shunt	Pneumonia, PE, ARDS, ILD
Type II	Low (< 8 kPa)	High (> 6 kPa)	Alveolar hypoventilation	COPD exacerbation, neuromuscular disease, chest wall disease, drug overdose

Why does Type I have normal/low CO2? Because CO2 diffuses 20× faster than O2 across the alveolar membrane. In V/Q mismatch, hyperventilation of well-ventilated areas compensates for CO2 elimination but cannot fully compensate for O2 (due to the shape of the oxyhaemoglobin dissociation curve — the flat upper portion means hyperventilation adds minimal extra O2 to already-saturated blood).

Why does Type II have high CO2? Because the problem is ventilation itself — the patient cannot move enough air in and out of the lungs, so both O2 delivery AND CO2 removal are impaired.

From the 2023 minicase ABG question ^[8]:

pH 7.28, PaO2 8.0 kPa, PaCO2 7.0 kPa, HCO3 35 mmol/L, BE -6
Interpretation: Type II respiratory failure (low PaO2 + high PaCO2) with partially compensated respiratory acidosis (pH still acidic but HCO3 elevated indicating chronic renal compensation)
Management: NIPPV (non-invasive positive pressure ventilation) or invasive mechanical ventilation ^[8]

Pulse oximetry: SaO2 & pulse rate, non-invasive, continuous & real-time. ABG: pH, PaO2, PaCO2, bicarbonate (much more complete acid-base picture), invasive, not continuous/real-time. ^[1]

Feature	Pulse Oximetry	ABG
Parameters	SaO2, pulse rate	pH, PaO2, PaCO2, HCO3, BE, lactate
Invasiveness	Non-invasive (clip on finger)	Invasive (arterial puncture — radial/femoral)
Continuous	Yes	No (single time-point)
When to use	Screening, monitoring	Suspected respiratory failure, acid-base derangement
Limitations	Can't assess CO2 or acid-base; unreliable in poor perfusion, nail polish, CO poisoning	Painful, risk of haematoma, single snapshot

High Yield: When to Order ABG vs Oximetry

If SaO2 is normal on oximetry and you just need monitoring → oximetry is sufficient. If you suspect Type II respiratory failure (e.g. drowsy COPD patient), you must get an ABG because oximetry cannot tell you the PaCO2. The 2023 minicase specifically tested ABG interpretation in a COPD patient. [1, 8]

5. Illustrative Test Questions from the Lecture

6. Integration: How Past Paper Questions Test This Lecture

Past Paper	Question Theme	Key Points from This Lecture
2022 SAQ Q2	Massive right pleural effusion — name 4 respiratory symptoms, 2 systemic symptoms, 4 physical signs	5 major symptoms (cough, sputum, haemoptysis, dyspnoea, chest pain); systemic = weight loss, fever; signs = stony dull percussion, reduced breath sounds, reduced expansion, tracheal deviation away
2022 SAQ Q6	Smoker with cough + mucoid sputum + exertional dyspnoea — most likely diagnosis and DDx	COPD (chronic obstructive pulmonary disease) in acute exacerbation; DDx = asthma, bronchiectasis, lung cancer, pneumonia
2023 Minicase Case 1	Construction worker + smoker + old TB — physical signs, CXR findings, investigations, spirometry, ABG	Physical signs from this lecture (clubbing, crackles, hyperexpansion); spirometry interpretation (obstructive, no reversibility); ABG (Type II RF)
2024 SAQ Q4	Chronic smoker with cough — 5 cardiorespiratory comorbidities	COPD, lung cancer, IHD, heart failure, bronchiectasis
2025 SAQ Q3	Smoker with cough + haemoptysis + left apical mass — symptoms, signs, clinical syndromes	Symptoms from this lecture; signs = clubbing, LN, Horner; syndromes = SVCO, Pancoast

Question Stem	Mark Scheme Points
Name the five major pulmonary symptoms	Cough, sputum, haemoptysis, dyspnoea, chest pain/discomfort
Name four causes of acute dyspnoea with chest pain	Pneumothorax, PE, pneumonia with pleuritis, acute MI/pulmonary oedema
Name three pulmonary causes of finger clubbing	Lung cancer, bronchiectasis, lung abscess, empyema, idiopathic pulmonary fibrosis
Differentiate obstructive from restrictive pattern on spirometry	Obstructive: FEV1/FVC < 70%; Restrictive: FEV1/FVC ≥ 70% but both FEV1 and FVC reduced
Define Type I and Type II respiratory failure	Type I: PaO2 < 8 kPa with normal/low PaCO2; Type II: PaO2 < 8 kPa with PaCO2 > 6 kPa
What does DLCO measure and name two conditions where it is reduced	Measures alveolar gas transfer; reduced in pulmonary fibrosis and emphysema
Name four drugs that can cause respiratory complications and state the effect	Aspirin (worsen asthma), beta-blockers (worsen asthma/COPD), corticosteroids (increase TB), amiodarone (pulmonary fibrosis)
Describe the percussion note and breath sounds expected in pleural effusion vs consolidation	Effusion: stony dull, reduced/absent breath sounds, reduced VR. Consolidation: dull, bronchial breathing, increased VR
A 65-year-old smoker with haemoptysis — name three causes to exclude	Lung cancer, TB, bronchiectasis
Interpret ABG: pH 7.28, PaO2 8.0, PaCO2 7.0, HCO3 35	Type II respiratory failure, partially compensated respiratory acidosis (renal compensation raising HCO3)

High Yield Summary

The respiratory clinical approach is: History → Examination → Investigations → Diagnosis → Management.

History: Five major symptoms (cough, sputum, haemoptysis, dyspnoea, chest pain). Always get TOCC (Travel, Occupation, Contact, Cluster). Drug history is critical: aspirin/beta-blockers worsen asthma; corticosteroids reactivate TB; amiodarone causes fibrosis.

Examination: General (distress, cyanosis, clubbing, oedema — bilateral = cor pulmonale, unilateral = DVT, cervical LNs). Chest: Inspection (scars, shape, symmetry) → Palpation (expansion, trachea) → Percussion (resonant = normal, dull = consolidation/collapse, stony dull = effusion, hyper-resonant = pneumothorax) → Auscultation (coarse crackles = bronchiectasis, fine crackles = fibrosis, wheeze = obstruction, bronchial breathing = consolidation).

Investigations: Blood (CBP, serology), Sputum (Gram, ZN, culture, cytology, PCR), NPA (viral molecular tests), Pleural fluid (Light's criteria, ADA), Imaging (CXR — may miss retrocardiac/mediastinal lesions; CT for nodules/LNs), Lung function (PFR/Spirometry → airway; DLCO → alveoli; ABG/oximetry → respiratory failure), Bronchoscopy (central lesions), CT-guided biopsy (peripheral lesions), Polysomnography (OSA).

Respiratory failure: Type I = low PaO2, normal/low PaCO2 (oxygenation failure). Type II = low PaO2 + high PaCO2 (ventilatory failure).

Spirometry: Obstructive = FEV1/FVC < 70%. Restrictive = FEV1/FVC ≥ 70% but both values low.

CFB MED03 Respiratory System

Respiratory System: Introduction — CFB (MED03) Comprehensive Exam-Ready Notes

2. History Taking — Detailed Breakdown

HPI Example (from lecture) [1]

3. Physical Examination of the Respiratory System

4. Investigations in Respiratory Disease

4.6 Lung Function Tests

5. Illustrative Test Questions from the Lecture

6. Integration: How Past Paper Questions Test This Lecture

Active Recall - Respiratory System Introduction

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CFB MED03 Respiratory System

Respiratory System: Introduction — CFB (MED03) Comprehensive Exam-Ready Notes

Lecture Map: The Big Idea

Master Workflow Diagram

1. The Clinical Approach in Medicine

2. History Taking — Detailed Breakdown

2.1 Structure of the Respiratory History

HPI Example (from lecture) [1]

2.2 Major Pulmonary Symptoms (Chief Complaints)

2.3 Symptom Assessment Framework

2.4 Cough & Sputum — Temporal Classification

2.5 Common Causes of Dyspnoea

2.6 Common Causes of Haemoptysis

2.7 TOCC History

2.8 Drug History — Respiratory Side Effects

3. Physical Examination of the Respiratory System

3.1 General Examination

3.2 Important Pulmonary Causes of Clubbing

3.3 Chest Examination: Inspect, Palpate, Percuss, Auscultate

3.4 Additional Examination Findings from Supporting Material [3, 4]

4. Investigations in Respiratory Disease

4.1 Blood Tests

4.2 Sputum Analysis

4.3 Nasopharyngeal Aspirates (NPA)

4.4 Pleural Fluid Analysis

4.5 Imaging

4.6 Lung Function Tests

4.6.1 Peak Flow Rate (PFR)

4.6.2 Spirometry (FEV1/FVC)

4.6.3 Diffusing Capacity (DLCO)

4.6.4 Concept of Respiratory Failure

4.6.5 Pulse Oximetry vs ABG

4.7 Bronchoscopy

4.8 Transthoracic Fine Needle Aspirate/Biopsy

4.9 Polysomnography

5. Illustrative Test Questions from the Lecture

Test 1 (from slide) [1]:

Test 2 (from slide) [1]:

6. Integration: How Past Paper Questions Test This Lecture

6.1 SAQ Patterns [7, 8, 9, 10, 11]

6.2 Common Exam Traps

7. Likely Exam Questions

8. High Yield Summary

Active Recall - Respiratory System Introduction

References

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